In brain ischemia/reperfusion injury, BTK was required for NLRP3 inflammasome-dependent IL-1β processing in macrophages and BTK inhibition effectively impaired NLRP3 inflammasome activation and efficiently improved neurological function [15] In terms of mechanisms, BTK can physically interact with NLRP3 and ASC, resulting in the induction of ASC oligomerization and caspase-1 activation in vitro [15]. The gene discussed is NLRP3; the disease is brain ischemia.